Skeletal and cardiac myopathy in HIV-1 transgenic rats

The mechanism by which human immunodeficiency virus (HIV)-1 infection in humans leads to the erosion of lean body mass is poorly defined. Therefore, the purpose of the present study was to determine whether transgenic (Tg) rats that constitutively overexpress HIV-1 viral proteins exhibit muscle wasting and to elucidate putative mechanisms. Over 7 mo, Tg rats gained less body weight than pair-fed controls exclusively as a result of a proportional reduction in lean, not fat, mass. Fast- and slow-twitch muscle atrophy in Tg rats did not result from a reduction in the in vivo-determined rate of protein synthesis. In contrast, urinary excretion of 3-methylhistidine, as well as the content of atrogin-1 and the 14-kDa actin fragment, was elevated in gastrocnemius of Tg rats, suggesting increased muscle proteolysis. Similarly, Tg rats had reduced cardiac mass, which was independent of a change in protein synthesis. This decreased cardiac mass was associated with a reduction in stroke volume, but cardiac output was maintained by a compensatory increase in heart rate. The HIV-induced muscle atrophy was associated with increased whole body energy expenditure, which was not due to an elevated body temperature or secondary bacterial infection. Furthermore, the atrophic response could not be attributed to the development of insulin resistance, decreased levels of circulating amino acids, or increased tissue cytokines. However, skeletal muscle and, to a lesser extent, circulating insulin-like growth factor I was reduced in Tg rats. Although hepatic injury was implicated by increased plasma levels of aspartate and alanine aminotransferases, hepatic protein synthesis was not different between control and Tg rats. Hence, HIV-1 Tg rats develop atrophy of cardiac and skeletal muscle, the latter of which results primarily from an increased protein degradation and may be related to the marked reduction in muscle insulin-like growth factor I.     

Teratogenicity of carbamazepine in rats

The teratogenicity of carbamazepine (CBZ) was investigated in Sprague-Dawley CD rats at doses of 0, 200, 400, and 600 mg/kg administered by gavage in corn oil on days 7-18 of gestation in a dosage volume of 2 ml/kg. The CBZ-600 dose was maternally toxic in that dams in this group weighed 30.6% less than controls by E20. This group had significantly increased resorptions, reduced live fetal weight (51.6% less than controls), and increased skeletal and visceral abnormalities. The CBZ-400 dose also significantly reduced maternal weight gain during gestation to 26.6% less than controls by E20. No significant increase in resorptions occurred in this group; live fetuses weighted 42.9% less than controls and showed an increase in visceral, but not skeletal, abnormalities. The CBZ-200 dose did not significantly affect maternal weight gain or increase resorptions or fetal abnormalities but did reduce fetal body weight (20.3% less than controls). Maternal serum total CBZ concentrations 1 hr after the final dose were 22.9, 27.9, and 34.4 micrograms/ml for the 200, 400, and 600 mg/kg groups, respectively. These levels were little changed 6 h post-treatment. CBZ was 65-70% serum protein bound across dose groups. Human therapeutic levels of CBZ are 4-12 micrograms/ml and the drug is typically 80% serum protein bound. This suggests that abnormalities in rats occur at concentrations well above the human therapeutic range. However, a no-effect level was not found for fetal body weight. Further experiments will be required to determine how much lower doses will need to be in order to find a no-effect level for fetal body weight. Nevertheless, the present data suggest that CBZ is not potent at inducing malformations in rats.     

Effect of Triethyl Tin on Myelination in the Developing Rat

Myelinogenesis in developing rats was studied following chronic dosing with triethyl tin (TET), at a level of 1.0 mg TET/kg body wt/day. Experiments included starved controls with body weights depressed by 17 to 40% to equal those of the TET-treated groups. Rats at ages of 16, 21, and 30 days showed decreases relative to well-nourished controls in body weight, forebrain weight, myelin yield, cerebroside level, and specific activity of brain 2',3'-cyclic nucleotide-3'-phosphohydrolase when dosed with TET. At 30 days, myelin and cerebroside yields were reduced by approximately 55%, while CNP activity was reduced by less than 20%. No differences in the forebrain myelin protein composition between control, starved, and TET animals were noted. The rate of myelin protein synthesis relative to brain total protein (assayed by incorporation of intracranially injected [3H]glycine into brain homogenate and myelin proteins) was decreased in the TET rats in proportion to the decreased yield of myelin, but no particular myelin protein was preferentially affected. Matching starved controls exhibited similar body weight decreases, less pronounced forebrain weight decreases, and little or no decrease in myelin concentration. There was a relative increase in the myelin protein synthesis rate in the starved rats, indicating preferential utilization of limited protein precursors for myelin protein synthesis. Spinal cord myelin was also decreased in the TET rats, but less severely than in the forebrain. At all ages optic, but not sciatic, nerves showed decreases in myelin concentration with TET treatment. We conclude that TET inhibits forebrain growth and CNS myelination more severely than can be accounted for by a general metabolic insult.     

Preferential loss of body fat during starvation in dietary obese rats.

This study was undertaken to examine whether diet-induced obesity alters the amount and/or composition of weight lost during starvation. The amount and composition of weight lost during a 4-day period of starvation was determined before and at 17, 30 and 42 weeks after rats (350 g of body weight) were given a high fat diet (HFD). To control for effects of aging, a second group of rats, fed standard laboratory chow, was also subjected to similar periods of starvation. Although total weight loss during starvation was never greater for HFD rats than for chow-fed rats, the former group showed a clear patter of increasing loss of body fat and total energy and conservation of fat-free tissues with periods of starvation later in life. In addition, chow-fed rats showed substantial energy conservation during each period of starvation (i.e. they lost less energy each day than their pre-starvation energy requirements). In contrast, HFD rats demonstrated substantial energy conservation only at 17 weeks and not at 30 or 42 weeks; during the last period of starvation, their average daily loss of carcass energy exceeded their pre-starvation energy requirements. This suggests the increased fat mass of these rats may have led to increased fuel availability and to an increased metabolic rate during starvation. If these results are applicable to humans, the more obese subjects are likely to show greater total loss of energy than lean subjects, but show a lesser loss of lean body mass, at least initially. If protein requirements are reflected by the ability to mobilize protein during food restriction, protein requirements would be substantially lower in the dietary obese rats than in controls. In summary, diet-induced obesity leads to preferential loss of body fat and conservation of lean mass during starvation.     

Effect of structured lipid-enriched total parenteral nutrition in rats bearing yoshida sarcoma

The efficacy of structured lipid, a triacylglycerol of medium and long chain fatty acids, as an element of nutritional support therapies in cancer cachexia was investigated. Using the Yoshida sarcoma to induce cachexia, male Sprague Dawley rats (90 g) were injected subcutaneously with tumor cells (n = 17) or sterile saline (n = 16). Seven days later, rats were randomized to two intravenous diets for 3 days at 220 kcal/kg body weight/d, including 2 g nitrogen/kg body weight/d and 39% of total calories as either structured lipid or long chain triglyceride. Nitrogen balance, tumor growth rate, energy metabolism, and plasma albumin and free fatty acid levels were measured, and whole-body protein kinetics and liver, muscle, and tumor fractional protein synthetic rates were evaluated by adding (14)C-leucine to the diet during the last 4 hours of feeding. Nitrogen balance improved (P < .05) in both tumor and control rats receiving structured lipid-enriched total parenteral nutrition, and was also greater in tumor rats compared with controls. There were no differences in tumor growth or protein kinetics between diet groups. Albumin was lower (P < .05) in tumor rats, but significantly higher in both tumor and control rats given structured lipid-enriched total parenteral nutrition. Free fatty acid was significantly higher in tumor rats versus controls. Whole-body protein kinetics were similar among the four groups. Liver weight, liver weight to body weight ratio, and liver protein synthetic rate were higher in tumor rats. Also, liver weight to body weight ratio was lower in tumor and control animals given structured lipid-enriched total parenteral nutrition. Muscle protein synthetic rate was significantly lower in tumor rats, but higher in tumor and control rats given long chain triglyceride-enriched total parenteral nutrition. The nutritional benefits of structured lipid-enriched total parenteral nutrition favor support of host tissue without promoting tumor growth.     

Adipose tissue development, growth, and food consumption in protein-malnourished rats.

Effects of protein malnutrition on adipose tissue development were studied in weanling male Sprague-Dawley rats fed isocaloric diets ad libitum containing either 22% (controls) or 8% (protein-malnourished rats) casein, and in rats pair-fed to the protein-malnourished rats with the 22% casein diet. After 32 days on the diet, protein-malnourished rats were 37% and pair-fed 67% the weight of the controls, while torso length was 37% and 73% of controls, respectively. Food consumption relative to body weight was greatest in protein-malnourished rats. Compared to control rats, the distal epididymal adipocyte number in the protein-malnourished rats was decreased in proportion to the decrease in body size and was more closely related to the protein intake than to the total calories consumed. After 32 days on diet, mean adipocyte number per 2 distal pads was 11.7 x 10(6) in controls and 4.3 x 10(6) in protein-malnourished rats. In pair-fed rats, cell number lagged behind controls at 4 and 11 days, but was normal at 32 days (11.4 x 10(6) cells). The distal epididymal pad adipocyte size and percent lipid were similar in all groups during the first 25 days of dietary treatment. Adipocyte size was increased significantly in controls at day 32 compared to the other two groups. At each time studied through day 25 on diet, epididymal pad weight was related to the adipose cell number rather than the cell size. It is concluded that severe restriction of dietary protein during the postweaning period of growth in rats results in decreased epididymal adipocyte proliferation and/or differentiation concomitant with generalized growth retardation, whereas isocaloric feeding of a diet of normal protein content is associated with only a transient delay in adipose tissue development.     

Effects of clenbuterol on insulin resistance in conscious obese Zucker rats

The present study was conducted to determine the effect of chronic administration of the long-acting beta(2)-adrenergic agonist clenbuterol on rats that are genetically prone to insulin resistance and impaired glucose tolerance. Obese Zucker rats (fa/fa) were given 1 mg/kg of clenbuterol by oral intubation daily for 5 wk. Controls received an equivalent volume of water according to the same schedule. At the end of the treatment, rats were catheterized for euglycemic-hyperinsulinemic (15 mU insulin. kg(-1). min(-1)) clamping. Clenbuterol did not change body weight compared with the control group but caused a redistribution of body weight: leg muscle weights increased, and abdominal fat weight decreased. The glucose infusion rate needed to maintain euglycemia and the rate of glucose disappearance were greater in the clenbuterol-treated rats. Furthermore, plasma insulin levels were decreased, and the rate of glucose uptake into hindlimb muscles and abdominal fat was increased in the clenbuterol-treated rats. This increased rate of glucose uptake was accompanied by a parallel increase in the rate of glycogen synthesis. The increase in muscle glucose uptake could not be ascribed to an increase in the glucose transport protein GLUT-4 in clenbuterol-treated rats. We conclude that chronic clenbuterol treatment reduces the insulin resistance of the obese Zucker rat by increasing insulin-stimulated muscle and adipose tissue glucose uptake. The improvements noted may be related to the repartitioning of body weight between tissues.     

Effects of semi-starvation on the total body composition and absorptive function of the small intestine of the young adult female rat.

Sixteen female rats aged about 80 days and with a mean body weight of 175 g were fed 40% of their ad libitum intake of a laboratory chow. They were killed and analysed for water, protein, lipid and ash after 9, 21-5, 30-2 and 38-8% of body weight had been lost. Compared to a control group of four animals, the 38-8% group lost 13 g or 34% of their protein. The animals in the 21-5, 30-2 and 38-8% groups lost 7-5 g or 87% of their lipid leaving only 1-1 g of lipid. The percentage protein in the body was little affected by body weight loss but lipid decreased from 5 to 1%. In another experiment with 26 rats of 205 g mean body weight and aged about 115 days, absorption rates by the small intestine were measured in vivo after variable weight losses between 0 and 39%. D(+)-Glucose uptake was increased by about 70% in those animals which had lost only 5% of body weight and this increased uptake was retained in those rats which had lost up to 39% of body weight. The absorption of L-leucine was not affected by the decline in body weight compared to the controls but relative to body weight, the ability of the intestine to absorb increased. In the same animals, the wet and dry weights of the small intestine declined slightly faster than body weight and the length of the small intestine tended to decrease slightly with increasing loss of body weight.     

Evidence for increased peroxidative activity in muscles from streptozotocin-diabetic rats

The ability of cardiac and skeletal muscles from diabetic rats to metabolize superoxide and hydrogen peroxide was determined by the activities of superoxide dismutase (SOD) and catalase, respectively. Male and female Sprague-Dawley rats, 43 days old, were made diabetic with a single intravenous injection of streptozotocin (70 mg/kg body weight). On the 80th day after injection the blood glucose concentration of these rats was increased fourfold, and the plasma insulin concentration was decreased four- to fivefold compared to controls. Body weights of male diabetic rats were 61% and those of female diabetic rats were 66% of their ad libitum-fed controls. The seven different skeletal muscles examined weighed less in the diabetic rats than in controls of the same age and body weight. The hearts of the diabetic rats weighed more than those of controls of the same age and body weight. Comparison to the body weight controls allowed the distinction of specific effects due to lack of insulin from effects due to retardation in muscle growth. Increased catalase activity in all muscles examined from diabetic rats (plantaris, gastrocnemius, and heart) suggested a response in catalase activity similar to that of starved rats. SOD activity was not altered in the diabetic rat skeletal muscles and erythrocytes, but was somewhat decreased in the heart.     

Mirex-induced liver enlargement in rats is dependent upon an intact pituitary-adrenalcortical axis

The effect of prior hypophysectomy upon mirex-induced liver hypertrophy in male Sprague-Dawley rats was examined. Mirex had no effect upon adrenal weight, liver weight, plasma glucose or plasma corticosterone in hypophysectomized rats. However, daily corticosterone supplements (20 mg/kg body weight, sc) given to mirex-treated hypophysectomized animals yielded a 52% increase in liver weight to body weight ratios over those observed in mirex-treated hypophysectomized animals not receiving supplement. In intact rats, both liver weight to body weight ratios and plasma ACTH were significantly increased over controls 2 days after mirex treatment. These results indicate that mirex-induced liver enlargement not only requires corticosterone, but that the response is dependent upon an intact pituitary-adrenalcortical axis.     

Fatty acid oxidation and fatty acid synthesis in energy restricted rats

The importance of fat oxidation and fatty acid synthesis were examined in rats fed approximately one half their ad libitum food intake for a period of 13 days followed by 7 days of ad libitum feeding (refed rats). This study was undertaken because previous reports demonstrated that refed rats rapidly accumulated body fat. Our results confirmed this observation: refed rats accrued body fat and body weight at rates that were approximately 3 times higher than controls. Evidence for a period of increased metabolic efficiency was demonstrated by measuring the net energy requirement for maintenance over the refeeding period: refed rats had a reduced metabolic rate during the period of energy restriction (approximately 30% lower than control) and this persisted up to 2 days after the reintroduction of ad libitum feeding. The major factor responsible for the rapid fat gain was a depressed rate of fatty acid oxidation. Calculations of protein and carbohydrate intake over the refeeding period showed that the simplest explanation for the decrease in fatty acid oxidation is fat sparing. This is possible because of the large increase in dietary carbohydrate and protein intake during the refeeding period when metabolic rates are still depressed. The increased carbohydrate and protein may adequately compensate for the increasing energy requirements of the ER rats over the refeeding period affording rats the luxury of storing the excess dietary fat energy.     

Metabolic effects of medium chain triglyceride-enriched total parenteral nutrition in rats bearing Yoshida sarcoma

The ability of medium chain triglyceride-enriched total parenteral nutrition to support host tissue in a model of cancer cachexia was assessed by measuring tumor growth, body weight, nitrogen balance, energy expenditure, leucine kinetics, fractional protein synthetic rate of tumor, liver, and abdominis rectus muscle, and plasma levels of glucose and albumin. Male Sprague-Dawley rats (85-90 gm) received 10(7) cells of viable Yoshida sarcoma subcutaneously on day 0. Control rats received injections of sterile saline. On day 10 rats underwent central venous cannulation and were randomized to one of three isocaloric diets. One group received amino acids and dextrose, while the other two groups were infused with amino acids, dextrose, and fat as either long chain triglyceride or a physical mixture of medium chain triglyceride: long chain triglyceride (3:1). On day 14 L-1-(14)C-leucine was added to the diet to study protein kinetics, and energy metabolism was measured by indirect calorimetry. Both tumor-bearing and nontumor-bearing rats demonstrated improved nitrogen balance when given medium chain triglyceride-enriched total parenteral nutrition. Tumor-bearing rats had reduced resting energy expenditure vs. nontumor-bearing, while rats receiving total parenteral nutrition without fat had significantly greater respiratory quotients. Tumor-bearing rats had lower total body weight vs. nontumor-bearing on day 10, but body weight of tumor-bearing and nontumor-bearing did not differ on day 14. Whole body protein breakdown decreased and leucine balance increased in tumor-bearing rats as compared to nontumor-bearing. Total liver mass was greater in tumor-bearing rats, but liver protein fractional protein synthetic rate decreased in tumor-bearing rats vs. nontumor-bearing. Tumor growth rate and fractional protein synthetic rate were not altered by the parenteral diet. The data confirm an altered metabolism in the tumor-bearing host, and suggest that medium chain triglyceride can better support host tissue.     

Gender-specific effects of thyroid hormones on cardiopulmonary function in SHHF rats.

Spontaneously hypertensive heart failure (SHHF) rats develop hypertension and heart failure. We hypothesized that induction of hyperthyroidism should accelerate development of heart failure in male SHHF rats. Male and female SHHF rats received diets containing desiccated thyroid glands (DTG) or a control diet for 8 wk. Male and female Wistar-Kyoto rats were used as normotensive controls. DTG treatment reduced body weight in male, but not female, SHHF rats but increased body temperature and heart weight-to-body weight ratio in both genders. In DTG-treated male SHHF rats, serum triiodothyronine levels doubled relative to SHHF controls, whereas O2 consumption increased in DTG-treated SHHF rats. Frequency of breathing in air increased in DTG-treated female rats, and ventilation increased in DTG-treated male rats. Ventilatory equivalents exhibited gender differences in SHHF rats, were decreased in both genders by DTG treatment, and reached levels similar to those of Wistar-Kyoto rats. DTG increased heart rate, right ventricular pressure, and contractility in both genders and increased left ventricular pressure in SHHF male rats. These results refute our hypothesis and suggest that cardiopulmonary function of SHHF male rats may be improved by DTG treatment.     

Decreased urea synthesis in cafeteria-diet-induced obesity in the rat.

Feeding rats with a cafeteria diet resulted in increases in total body weight and in epididymal-adipose-tissue weight. Those rats excreted significantly less N than did controls. The amount of N ingested by cafeteria-diet-fed rats was kept equal to that of controls. This decrease in N excretion is explained by a decrease in urinary excretion of urea. This may be due to the following facts. The rate of synthesis of urea from precursors by isolated hepatocytes from cafeteria-diet-fed rats was lower than in controls. In cafeteria-diet-fed rats the activities of all the enzymes of the urea cycle are decreased. The major percentage decreases are those of carbamoylphosphate synthetase (EC 6.3.4.16) and of argininosuccinate synthetase (EC 6.3.4.5), the enzymes probably involved in the regulation of the overall rate of the cycle. When rats are switched to normal chow diet, the enzyme activities return to normal values. The uptake of amino acids by liver of cafeteria-diet-fed rats is lower than in controls. These results contrast with those obtained previously by using other models of obesity in rat (i.e. genetic or hypothalamic), in which N excretion was increased.     

Dehydroepiandrosterone (DHEA) facilitates liver regeneration after partial hepatectomy in rats

In this study we investigated whether or not liver regeneration is facilitated by dehydroepiandrosterone (DHEA) after partial (70%) hepatectomy in rats. Treatment with DHEA (300 mg/kg body weight) did not cause any significant increase in the expression ratio of proliferating cell nuclear antigen (PCNA) in sham-operated controls; however, in partially hepatectomized rats it caused a significant increase in the ratio in hepatocytes 24 and 36 hr after hepatectomy. In partially hepatectomized rats, DHEA treatment significantly accelerated the restoration of liver 48, 60, and 72 hr after partial hepatectomy. The restoration rate in DHEA-treated hepatectomized rats at 72 hr was 1.3-fold greater than in partially hepatectomized controls. Treatment with androstenedione (300 mg/kg body weight), the first metabolite of DHEA, did not cause any significant increase in the expression of PCNA in either sham-operated controls or partially hepatectomized rats. These results indicate that DHEA itself promotes the liver regenerative process after partial hepatectomy in rats.     

Effects of physical training on rat myocardium. An enzymatic and ultrastructural morphometric study

Rats subjected to physical training through swimming increased their weight at a slower rate than controls, which initially had the same characteristics. The ratio heart weight/body weight was 23% greater in the trained rats. However, the absolute weights of the hearts were only 7% greater. The ultrastructural morphometric study, backed up by and analysis of the hierarchical variance, did not reveal significant changes neither in the myofibrillar and mitochondrial volume nor in the number of mitochondria per surface unit of myocardium. Furthermore, no variations were recorded, due to training, in the amount of mitochondrial protein nor in the specific mitochondrial activities of malate dehydrogenase, cytochrome c oxidase and ATPase. It is therefore suggested that the increase in the measured parameters, due to training, is proportional to the increase in weight and size of the heart. On the other hand, the specific activity of LDH increased by 15% after the first weeks of training.     

Effect of a selectiveβ 2-adrenergic agonist (Cenbuterol) on energy balance and body composition in normal and protein deficient rats

In rats fed a normal (22% protein) diet, injection of clenbuterol (1 mg/kg/d for 21 d) did not affect energy intake, energy expenditure or weight gain, but reduced energetic efficiency, and fat and energy gains and increased body protein content. Presenting a low-protein (8%) diet reduced energy intake, gain and efficiency, body protein content and the mass of the gastrocnemius muscle when compared to rats fed the control diet. Injection of the protein-deficient rats with clenbuterol (1 mg/kg/d for 21 d) caused hypophagia and reduced body weight and energy gains, energy expenditure and total body fat. However, the total body content of protein was not significantly reduced and the percentage of body protein in this protein deficient, clenbuterol-treated group was greater than that of untreated rats on both the high- and low-protein diets. The ratio of body protein to fat following clenbuterol treatment was increased by over 50% in both normal and protein-deficient rats. The results show that in protein deficient animals, clenbuterol treatment may help conserve body protein at the expense of fat, resulting in a smaller, but leaner body mass.     

Estrogenic regulation of body weight in the female rat.

For a period of weeks subsequent to bilateral ovariectomy, female rats given unlimited access to food increased their food intakes and the rates at which they gained body weight; this resulted in elevated levels of body weight. Restricting ovariectomized (ovx) rats to their preoperative level of food intake (restricted diet), prevented this excessive gain in body weight. Estradiol benzoate (EB) treatments of 0.5 μg per day for 15 consecutive days partially reversed pre-occurring weight gain in obese ovx rats; this was accompanied by a reduction in food intake. In contrast, identical EB treatment for nonobese ovx rats (restricted diet) did not result in any loss of body weight or change in food intake. Oil-treated nonobese ovx rats gained a small amount of weight relative to their EB-treated counterparts, despite the similarity in their food intakes. Thus, part of the increased weight gain observed after ovariectomy may be independent of changes in food consumption, and related to removal of estrogenic influences from metabolic and behavioral processes involved in energy balance. The weight limiting actions of estradiol were far more pronounced in animals already obese or facing impending obesity than in animals in which excessive weight gain was prevented. The data also suggest that estradiol is more effective in preventing than in reversing the weight gain associated with ovariectomy, and that estrogenic influences on the body weight set point are manifested with very short latencies. These findings support earlier conclusions that estradiol does not regulate food intake directly, but secondarily controls consumption as a means of weight regulation.     

Protein appetite is increased after central leptin-induced fat depletion

Leptin reduces body fat selectively, sparing body protein. Accordingly, during chronic leptin administration, food intake is suppressed, and body weight is reduced until body fat is depleted. Body weight then stabilizes at this fat-depleted nadir, while food intake returns to normal caloric levels, presumably in defense of energy and nutritional homeostasis. This model of leptin treatment offers the opportunity to examine controls of food intake that are independent of leptin's actions, and provides a window for examining the nature of feeding controls in a "fatless" animal. Here we evaluate macronutrient selection during this fat-depleted phase of leptin treatment. Adult, male Sprague-Dawley rats were maintained on standard pelleted rodent chow and given daily lateral ventricular injections of leptin or vehicle solution until body weight reached the nadir point and food intake returned to normal levels. Injections were then continued for 8 days, during which rats self-selected their daily diet from separate sources of carbohydrate, protein, and fat. Macronutrient choice differed profoundly in leptin and control rats. Leptin rats exhibited a dramatic increase in protein intake, whereas controls exhibited a strong carbohydrate preference. Fat intake did not differ between groups at any time during the 8-day test. Despite these dramatic differences in macronutrient selection, total daily caloric intake did not differ between groups except on day 2. Thus controls of food intake related to ongoing metabolic and nutritional requirements may supersede the negative feedback signals related to body fat stores.     

Acetaldehyde and cardiac protein synthesis in the rat in vivo

Protein synthesis was measured in the hearts of rats exposed to acetaldehyde vapour for 21 days. Exposure to acetaldehyde significantly increased heart weight (expressed as % body weight) but was without effect on the rate of synthesis of mixed cardiac proteins. Concentrations of RNA in the hearts were not altered by acetaldehyde exposure, indicating no change in RNA activity for protein synthesis.